arrhythmias), regardless of anatomy or patient size (smallest 25 kg). Mul-tiple chambers were mapped in 4 patients. In 7 patients a 64-electrodebasket catheter was deployed to facilitate assessment of target sites. Ab-lation was successful in 15/16 patients and 16/19 targeted arrhythmias. In1 patient, EAM data was utilized to perform successful intraoperativecryoablation for ventricular tachycardia during CHD repair. At mean fol-low-up 6.1 months (range 1-11 months), no ablated arrhythmias haveoccured, and no complications were observed. We conclude that theRPMTM is a viable electroanatomic mapping system in young patients andthose with complex CHD. Alternative reference catheter sites may berequired in small patients and those with complex venous and intracardiacanatomy. This stand-alone recording system is well-suited for use with a64-electrode basket catheter which serves as a useful adjunct to the EAMdata.

AB28-6

RIGHT VENTRICULAR FIBROSIS AND DISPERSION OFVENTRICULAR REPOLARIZATION IN PATIENTS WITHMUSTARD PROCEDURE FOR TRANSPOSITION OF THE GREATARTERIESOmer Goktekin, MD, Sonya Babu-Narayan, MD, Arif AnisKhan, MD, Anselm Uebing, MD, Philip J. Kilner, MD,Jonathan R. Clague, MD, PhD, Richard Sutton, MD andMichael A. Gatzoulis, MD, PhD. Osmangazi University,Eskisehir, Turkey and Royal Brompton Hospital, NationalHeart and Lung Institute, Imperial College, London, UnitedKingdom.

Background: Sudden cardiac death is a late complication in patients whoundergo atrial repair of transposition by Mustard/Senning procedure (2-15%). Fibrosis of right ventricular (RV) due to long term systemic pres-sure, which can be visualised by cardiovascular magnetic resonance, maylead to ventricular depolarization and repolarization abnormalities. The aimof the present study was to examine the possible relation between RVfibrosis and electrophysiological abnormalities of electrical depolarizationand repolarization in patients who have undergone the Mustard procedure.Methods: Thirty six patients (mean age 27, range 15-37 years), 21 males,who had undergone atrial redirection surgery (mean follow-up 24�6 years)were imaged by cardiovascular magnetic resonance with late gadoliniumenhancement. A single observer who was blind to the clinical data madeECG measurement. QRS, QT, and JT duration and QRS, QT and JTdispersion were measured manually from the standard 12 lead ECG using,digital calipers.Results: Late gadolinium RV enhancement showed myocardial fibrosisoccurred in 22 (61%) patients with various patterns. Patients with fibrosiswere older (30 vs 22 years p�0.001) and had increased QRS duration (108vs 98 ms, p�0.01), and QT dispersion (93 vs 71 ms, p�0.002) and also JTdispersion (100 vs 76 ms, p�0.001). The extent of fibrosis also correlatedwith age (r�0.59, p�0.001), QRS duration (r�0.67, p�0.001) and QTdispersion (r�0.38, p�0.02).Conclusion: Right ventricular myocardial fibrosis may play a crucial rolein the aetiology of sudden cardiac death on the basis of dispersion ofventricular depolarization-repolarization in patients with systemic rightventricle.

ABSTRACT SESSION 29: BASIC/TRANSLATIONAL SCIENCE V: ComputerModeling/SimulationFriday, May 6, 20058:15 a.m.–9:45 a.m.

AB29-1

FUNCTIONAL ATRIAL CONDUCTION ALTERNANS GENERATEDBY RAPID FOCI IN HOMOGENEOUS VIRTUAL HUMAN ATRIALTISSUEHenggui Zhang, PhD, Clifford J. Garratt, MD, Jiujinag Zhu,PhD and Arun V. Holden, PhD. The University of

Manchester, Manchester, United Kingdom and The Universityof Leeds, Leeds, United Kingdom.

Background: Rapid atrial focal excitation (FE) can initiate functionalre-entrant circuits leading to fibrillation. The transition between the 2 formsof activity is dependent on significant intrinsic and/or functional heteroge-neity (FH) in atrial properties that result in asymmetric atrial conduction.The mechanisms underlying the genesis of FH in conduction from rapidlyfiring atrial FE are unknown.Methods: The standard S1-S2 stimulus protocol with varied time intervals(SIs) was applied to a cell model of human atrial action potential (AP)developed by Courtemanche et al. (1998) to characterise the APD(90)restitution curve and its slope. 1D and 2D virtual human atrial tissues withhomogeneous electrical coupling between cells were constructed by incor-porating the cell model into a parabolic partial differential equation (PDE).FE waves were triggered by a series of periodic stimuli delivered to a localsite (with size/radius 1 mm). A focus period (FP) was chosen close to SIwhere APD(90) restitution curve has a slope above 1. AP and conductionvelocity (CV) were registered spatially across the tissue from beat to beat.Results: When SI � 350 ms, the APD(90) restitution curve had a slopegreater than 1. At low rates (FP � 400 ms), the FE waves propagateduniformally across the tissue and the registered APs and CVs showed nospatio-temporal differences. At high rates (FP � 325 ms), FE evoked APalternation in the tissue surrounding the focal source: a prolonged andlarger amplitude APs (APD(90)�280 ms) alternating with a shorter andsmaller APs (APD(90)�150 ms). The larger APs propagated relativelyfaster than the smaller ones, resulting in dynamic standing waves fluctu-ating irregularly in space and time. As a consequence, FH in atrial con-duction was produced, resulting in unstable spiral wave activity. Depend-ing on the relative distance between two recording sites, APs showed eithersynchronised or asynchronised alternans.Conclusion: High rate FE activity can produce a form of functional atrialconduction alternans in a structurally and functionally homogenous me-dium. This may constitute a novel mechanism whereby rapidly FE resultsin fibrillation.

AB29-2

PACEMAKER AND RE-ENTRANT ACTIVITY IN CONTRACTINGEXCITABLE MYOCARDIUMAlexandre V. Panfilov, PhD and Martyn P. Nash, PhD.University of Utrecht, Utrecht, Netherlands andBioengineering Institute and Department of EngineeringScience, University of Auckland, Auckland, New Zealand.

Mechano-electric feedback (MEF) is a complex concept that has been studiedin the clinical community for over a century, and may have arrhythmogenicconsequences. Mathematical modelling is a useful tool to study cardiac ar-rhythmogenesis, however most electrophysiological simulation studies havenot accounted for the mechanical function of the heart. Recently we introducedthe concept of a contracting excitable medium in order to study the basiceffects of mechanical deformations on re-entrant cardiac arrhythmias. It isbased on a modified Aliev-Panfilov 1996 ventricular excitation model with thenonlinear stress equilibrium equations that govern tissue mechanics. Thecoupled electromechanical model is solved using a hybrid approach thatincorporates finite difference and nonhomogeneous finite element techniquesfor the electrical activity and tissue mechanics, respectively. Here we study theeffects of mechanical activity on wave propagation in cardiac tissue. We showthat for some parameter values, MEF can induce automaticity in an array ofotherwise non-oscillatory cardiac cells, and illustrate the spatio-temporal dy-namics of these pacemakers. We also demonstrate the significant effects ofMEF on re-entrant wave dynamics. We found that contraction can induce driftof an otherwise stationary rotating spiral wave. This drift settles to an attractorthat can be located either at the center or periphery of the tissue, depending onits excitability. Finally, we observed that in some cases MEF can inducebreakup of a single re-entrant wave into complex fibrillatory patterns. Weconclude that tissue mechanics significantly contributes to the dynamics ofcardiac electrical activity, and that a coupled electromechanical-MEF frame-work should be adopted for future electrophysiological modelling studies.

S57Session 29